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x 2nd Year Medicine > Dermatology > Flashcards

Dermatology Flashcards

1
Q

What are the 4 layers of the skin from superficial to deep?

A

Epidermis
Basement Membrane Zone
Dermis
Subcutaneous layer

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2
Q

What are the 4 layers of the epidermis from superficial to deep?

A

Keratin layer
Granular layer
Prickle Cell layer
Basal layer

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3
Q

What do keratinocytes do?

A

Secrete a variety of cytokines in response to tissue injury or disease

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4
Q

In what layer are melanocytes found in?

A

Basal layer

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5
Q

Where does the epidermis originate from?

A

Ectoderm

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6
Q

What are the downward projections into the dermis from the epidermis called?

A

Rete Ridges

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7
Q

What are the 2 components of the epidermal cytoskeleton?

A

Keratin filaments

Desmosomal proteins

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8
Q

Which epidermal layer creates the semi-permeable skin barrier

A

Granular layer

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9
Q

What is the name of the skin cells which lose their nucleus in order to become surrounded by an inpermeable, protein envelope?

A

Stratum corneum cells

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10
Q

What types of immune molecules are involved in the innate immune system of the skin?

A

Netrophils, macrophages and keratinocytes

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11
Q

What can a deficiency in the skin’s innate immune system cause?

A

Atopic eczema

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12
Q

What is the role of melanocytes in the skin?

A

UV protection

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13
Q

Where are Merkel cells found?

A

Basal layer

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14
Q

What is the role of Merkel cells?

A

play a role in sensation esp. on fingertips and in the oral cavity

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15
Q

What are Langerhans cells?

A

Dendritic cells in the supra-basal layer; antigen presenting cells

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16
Q

What is the other name for the Basement Membrane Zone?

A

Dermo-epidermal junction (DEJ)

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17
Q

What does the basement membrane zone consist of?

A

Many types of collagen
Hemidesmosomal proteins
Integrins
Laminin

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18
Q

What is the role of the DEJ?

A

keeps the dermis and epidermis firmly attached

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19
Q

What can protein deficiencies in the DEJ cause?

A

Fragility of skin and a number of blistering diseases

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20
Q

Where does the dermis originate from?

A

Mesoderm

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21
Q

What does the dermis contain?

A

Blood, lymphatics, nerves, muscle

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22
Q

What is the dermis made of?

A

Collagen and Elastin in a ground substance

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23
Q

Where is the only surface Eccrine sweat glands are not found?

A

Mucosal surfaces

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24
Q

Where are the apocrine sweat glands found?

A

Axillae, anogential area, and scalp

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25
Q

What is the function of the sebaceous glands?

A

Secrete sebum (grease) onto the skin surface via the hair follicle - after puberty

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26
Q

How does hair form?

A

Downgrowth of epidermal keratinocytes into the dermis

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27
Q

What are the different parts of a hair shaft?

A

Inner and outer root sheaths, cortex, medulla

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28
Q

What are the 3 types of hair?

A

Terminal - scalp, beard, pubic
Vellus - fine downy hair on women’s faces and prepubescent children
Lanugo - Soft hair covering newborns (esp those premature)

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29
Q

What does the lower portion of the hair follicle consist of?

A

Expanded bulb (contains melanocytes), which surrounds a dermal papilla

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30
Q

What are the 3 stages of the hair growth cycle?

A

Anagen - growth phase
Catagen - involution phase
Telogen - Shedding phase

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31
Q

What causes hair to go grey?

A

decreased tyrosinase activity is hair bulb melanocytes

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32
Q

What causes hair to go white?

A

Total loss of melanocytes

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33
Q

What are nails?

A

Tough plates of hardened keratin

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34
Q

Where does nail growth arise from?

A

Nail matrix

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35
Q

What constitutes the subcutaneous layer?

A

Adipose tissue, blood vessels and nerves

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36
Q

Where do melanocytes originate from?

A

Neural crest

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37
Q

At what stage does a foetus have fully developed skin and hairs?

A

26 weeks

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38
Q

Histologically how is the epidermis described?

A

Stratified squamous epithelium

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39
Q

Histologically what is the basal layer made up of?

A

Once cell thick cuboidal cells

Intermediate filaments

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40
Q

What is the prickle cell made up of?

A

Polyhedral cells
Desmosomes
Keratohyalin granules

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41
Q

What does the keratin layer consist of?

A

Corneocytes
Keratin
Filaggrin

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42
Q

What is special about the cells of the oral mucosa?

A

Keratinised to deal with friction and pressure

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43
Q

What is special about the cells of the occular mucosa?

A

Lacrimal glands
Eye lashes
Sebaceous glands

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44
Q

Where do Melanocytes migrate from and to?

A

From the neural crest to the epidermis

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45
Q

What are melanocytes and where are they found?

A

Pigment-producing dendritic cells

In and above the basal layer

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46
Q

What colour is Eumelanin?

A

Brown or black

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47
Q

What colour is phaeomelanin?

A

Red/yellow

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48
Q

Where do Langerhans cells originate from?

A

Mesenchymal cells (bone marrow)

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49
Q

Where are Langerhan’s cells found?

A

Prickle cell layer (also dermis and lymph nodes)

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50
Q

How are Langerhans cells characterised histologically?

A

By Birbeck granules (they look like sports raquets)

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51
Q

Where are Merkel cells found?

A

Basal layer (between keratinocytes and nerve fibres)

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52
Q

What type of cell are Merkel cells?

A

Mechanoreceptors

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53
Q

What is dermographism?

A

Skin becomes raised and inflamed when stroked or scratched etc.

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54
Q

What causes dermographism (dermatographic urticarial)

A

Mast cells release histamines in the absence of antigens, due to their weak membranes

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55
Q

What can the sun do to the skin on a microscopic level?

A

Solar elastosis - elastin filaments break up and cause the skin to wrinkle

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56
Q

What receptors in the skin sense pressure changes?

A

Pacinian Corpuscles

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57
Q

What receptors in the skin sense vibrational changes?

A

Meissners Corpuscles

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58
Q

Under a microscope what do Pacinian Corpuscles look like?

A

sliced onion

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59
Q

Sebaceous glands are dormant at birth, when do they become active?

A

Puberty

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60
Q

What do sebaceous glands do?

A

Produce sebum to control moisture loss and to protect from bacterial and fungal infection

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61
Q

What causes acne?

A

Increased sebum production, blocked ducts and bacterial activity

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62
Q

Where would you find apocrine sweat glands?

A

Axillae and perineum

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63
Q

What do apocrine sweat glands do?

A

Produce an oily fluid which produces an odour after bacterial decomposition

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64
Q

What are apocrine sweat glands dependent on?

A

Androgens

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65
Q

Where do you find Eccrine sweat glands?

A

Whole skin surface; esp. palms, soles and axillae

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66
Q

What is the nerve supply to the eccrine sweat glands?

A

Sympathetic cholinergic nerve

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67
Q

What is the role of the eccrine glands?

A

Ultrafiltration of fluids
cooling by evaporation
Moistening palms and soles to aid grip

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68
Q

Give 2 examples of conditions considered as acute skin failure.

A

Toxic Epidermal necrolysis

Erythroderma

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69
Q

What to metabolic processes is the skin heavily involved in?

A

Vitamin D metabolism - Uv absorbed in skin helps in vit D metabolism

Thyroid Hormone metabolism - is 1 located of where T4 is converted to T4

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70
Q

What cells are important in the skin’s immune function?

A

Langerhan’s cells

T-Cells

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71
Q

What is impetigo?

A

A highly infectious skin disease which is most common in children

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72
Q

How does impetigo present clinically?

A

Weeping, exudative areas with a honey-coloured surface crust

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73
Q

How is impetigo spread?

A

Direct contact

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74
Q

What organisms can cause impetigo?

A

Staph

Group A beta-haemolytic strep

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75
Q

If impetigo is caused by a Staph infection, how is it treated?

A 
Oral antibiotics (7-10 days)
Flucloxacillin 500mg 4xdaily
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76
Q

If impetigo is caused by a Strep infection, how is it treated?

A

Phenoxymethylpenicillin 500mg 4xdaily (7-10 days)

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77
Q

If impetigo doesn’t respond to initial treatment what should then be done?

A

Nasal swabs taken

Nasal mupiocin 3xdaily (1 week) to eradicate nasal carriage

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78
Q

Staph infections can rarely release exfoliating toxins which act high up in the epidermal layer. What effects does toxin A produce if it is released?

A

Blistering at the infection site - bullous impetigo

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79
Q

Staph infections can rarely release exfoliating toxins which act high up in the epidermal layer. What effects does toxin B produce if it is released?

A

Staph Scalded Skin Syndrome (SSSS) - more widespread blistering

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80
Q

What groups are more at risk of developing SSSS?

A

Children
Immunosuppressed adults
Adults with renal disease

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81
Q

How are toxic infections released from Staph infections treated?

A

Flucloxacillin (with supportive care)

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82
Q

What is cellulitis?

A

A hot, tender area of confluent erythema due to deep subcut. infection (occasional blistering)

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83
Q

Where does cellultis often affect?

A

Lower leg (upward spreading)

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84
Q

What general symptoms will a patient with cellulitis have?

A

Generally unwell with a fever

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85
Q

What causes cellulitis?

A

Beta haemolytic strep or staph (rare)

Immunosuppressed/diabetic patients may develop gram -ve or anaerobic infection

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86
Q

How is cellulitis conformed/organism identified?

A

Serology

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87
Q

How is cellulitis treated?

A

Phenoxymethylpenicillin (or erythromicin) and flucloxacillin 500mg 4xdaily

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88
Q

What is ecthyma?

A

Chronic, well-demarcated, deeply ulcerative lesions (sometimes with an exudative crust)

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89
Q

What causes ecthyma

A

Strep or Staph infection

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90
Q

Ecthyma is rare in the UK, but what groups of patients may develop it?

A

IVDUs and HIV patients

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91
Q

What is the treatment for ecthyma?

A

Erythromicin PO 500mg 4xdaily for 7-10 days

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92
Q

What is erythrasma?

A

Orange-brown flexural rash - often seen in axillae or toe web spaces

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93
Q

What causes erythrasma?

A

Corynebacterium minutissimum

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94
Q

How does erythrasma appear under Wood’s light?

A

Coral pink fluorescence

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95
Q

How is erythrasma treated?

A

Erythromicin PO 500mg 4xdaily for 7-10 days

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96
Q

What is folliculitis and how does it present?

A

Inflammation of the hair follicle which presents with itchy, tender papules

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97
Q

What is the commonest causative organism of folliculitis?

A

Staph aureus

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98
Q

What is the treatment for folliculitis?

A

topical antiseptics and either topical or oral antibiotics

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99
Q

What are furuncles?

A

(Boils) are deep seated infections of the skin which present as painful, red swellings

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100
Q

What causes furuncles?

A

Staph infection

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101
Q

What should be done to ensure MRSA is not the cause of a furuncle?

A

Swabs for antibiotic sensitivities

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102
Q

How are furuncles treated?

A

Erythromicin 500mg 4xdaily for 10-14 days

Antiseptics (chlorhexidine) can be useful as prophylaxis

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103
Q

What is hidradentis suppurativa?

A

A painful, discharging, chronic inflammation in areas rich in apocrine glands of which there is no known cause

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104
Q

How is hidradentis suppurativa treated?

A

Weight loss, antibiotics and oral retinoids

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105
Q

What is pitted keratolysis?

A

A superficial infection of the horny layer of the skin caused by a corynebacterium

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106
Q

How does pitted keratolysis present?

A

On soles of feet with numerous, small, punched out lesions on a macerated (prune-like) skin

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107
Q

How is pitted keratolysis treated?

A

Topical antibiotics and anti-sweating lotions

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108
Q

How does leprosy present?

A

Rare in UK

Usually involves skin and the features depend on an individuals immune response to Mycobacterium leprae

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109
Q

What skin manifestations of TB are there?

A

Lupus vulgaris
Tuberculosis verrucoa cutis
Scrofuloderma
The tuberculides

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110
Q

What is viral exanthem?

A

The commonest type of viral-induced rash which presents as a widespread nonspecific erythamatous maculopapular rash.

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111
Q

What causes viral exanthem?

A

Circulating immune complexes of antibody + viral antigen localising to dermal blood vessels

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112
Q

What is Slapped Cheek Syndrome, and what causes it?

A

A rash across the face which can occur for weeks-months which is caused by Human Erythrovirus B19
Patient is generally well throughout and after the facial rash has cleared a lacy, macular rash appears on the body

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113
Q

Most people are affected by HSV1 in childhood and the majority have subclinical infection. If not however, how does this present?

A

Clusters of painful blisters on the face (esp around the mouth)

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114
Q

If HSV1 reccurs, how does it present?

A

Usually as cold sores

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115
Q

What does HSV2 infection typically cause?

A

Genital herpes

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116
Q

How is HSV infection treated?

A

Oral aciclovir 500mg 2xdaily for 5 days

Cold sores can be treated with topical aciclovir creams

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117
Q

What 2 diseases does varicella zoster virus cause?

A

Chicken pox - Varicella component

Shingles - Zoster componenet

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118
Q

How does chicken pox present?

A

Generlised itchy rash and fever

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119
Q

What complications can arise from chicken pox?

A 
secondary infection
pneumonia
haemorrhagic rash
scarring
encephalitis (brain tissue swelling)
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120
Q

How is chicken pox treated?

A

It isn’t usually - self limiting process

Infection = immunity in most cases

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121
Q

What causes shingles?

A

Reactivation of the virus, usually in older age in a dermatomal pattern

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122
Q

How does shingles present?

A

Preceded by a tingling sensation or pain

This is followed by a painful, tender, blistering erruption which occur in crops, become pustular and then crust over

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123
Q

How long does a shingles rash typically last for?

A

2-4 weeks

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124
Q

What complications can arise from shingles?

A

Severe, persistant pain

Others depending on the dermatome affected

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125
Q

How is shingles treated?

A

Analgesia and antibiotics (if secondary bacterial infection)

Valaciclovir1g or famciclovir 250mg 3xdaily for 7days (shortens attacks)

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126
Q

What does HPV cause relating to the skin?

A

Viral Warts

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127
Q

What are common HPV warts?

A

Papular lesions with a course, roughened surface often seen on the hands and feet.
They have small black dots (bleeding points)

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128
Q

How do HPV common warts spread?

A

Direct contact

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129
Q

What is another name for plantar warts caused by HPV?

A

Verrucae

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130
Q

What are plane warts?

A

Less common lesions caused by only certain types of HPV. Are very small, flesh coloured/pigmented and flat topped.

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131
Q

Where are plane warts typically found?

A

Face or backs of hands - usually in multiples

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132
Q

How are warts caused by HPV treated?

A

almost always resolve spontaneously
Topical keratolytic agents can speed up the healing process
Cryotherapy may also be helpful but it does have side effects

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133
Q

What is molluscum contagiosum?

A

A common cutaneous infection in childhood causing multiple small translucent papules which are solid to touch

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134
Q

What causes molluscum contagiosum?

A

The pox virus

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135
Q

How is molluscum contagiosum spread and how long does infection last?

A

Direct contact

6-12 months

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136
Q

What is orf?

A

A pox virus disease of sheep which can be spread to humans via direct contact

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137
Q

How does orf present?

A

1-2cm reddish papule with a surrounding erythema which usually becomes pustular

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138
Q

What is tinea corporis?

A

A dermatophyte fungal infection of the body

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139
Q

How does tinea corporis present clinically?

A

Asymmetrical scaly patches with central clearing and an advancing, scaly raised edge.

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140
Q

What is tinea faciel?

A

A dermatophyte fungal infection of the face

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141
Q

How does tinea faciel present?

A

Often occurs after topical steroid use
Erythematous, slightly scaly lesions
Itchy after sun exposure

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142
Q

What is tinea cruris?

A

A dermatophyte fungal infection of the groin

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143
Q

How does tinea cruris present?

A

Well-demarcated, red plaques with arc like borders, extending down from the upper thighs

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144
Q

What is tinea pedis?

A

A dermatophyte fungal infection of the feet

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145
Q

How does tinea pedis present?

A

Infection mainly in the toe clefts with white, macerated and fissured lesions

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146
Q

What is tinea manuum?

A

A dermatophyte fungal infection of the hands

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147
Q

How does tinea manuum present?

A

A diffuse, erythematous scaling of the palms and backs of hands
Variable skin peeling and thickening

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148
Q

What is tinea capitis?

A

A dermatophyte fungal infection of the scalp

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149
Q

How does tinea capitis present?

A

From a mild diffuse scaling with no hair loss, to scaly patches with associated alopecia.
May present with a few pustules with exudate

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150
Q

What is tinea unguium?

A

A dermatophyte fungal infection of the nails

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151
Q

How does tinea unguium present?

A

An asymmetrical discoloration of 1 or more nails

Nail plate appears thickened and a crumbly white material appears under it

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152
Q

What is tinea incognito?

A

A fungal skin infection modified by topical steroid use

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153
Q

How does tinea incognito present?

A

Variable - non-specific erythema or a few reddish nodules with a little scaling. Rash improves with steroids but gets and spreads when treatment is stopped

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154
Q

What is the treatment for all tinea infections?

A 
Body of flexures = topical antifungals
Widespread = oral antifungals
Toenails  Itraconazole (antifungal) for 3-6 months
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155
Q

What is Candida albicans?

A

An opportunistic yeast that thrives in warm and moist environments

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156
Q

How would a candida albicans infection present?

A

A superficial white/creamy psuedomembranous plaque which can be scraped off leaving raw areas underneath.
Satellite lesions may also be found

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157
Q

How is a candida albicans infection treated?

A

Topical antifungal creams

Nail infections need systemic antifungal therapy

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158
Q

What is pityriasis versicolour?

A

An overgrowth of the normal bacterial skin flora or pityrosporum

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159
Q

How does pityriasis versicolour present?

A

In white people - reddish-brown scaly lesions on the trunk

In black people - macular areas of hypopigmentation

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160
Q

How is pityriasis versiolour treated?

A

Slenium sulphide or 2% ketoconazole shampoo or topical imidazole cream

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161
Q

What is seborrhoeic eczema?

A

A pityrosporum folliculitis

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162
Q

How does seborrhoeic eczema present?

A

Small itchy papules on the upper back, centered on the hair follicles (common in young adult males)

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163
Q

How is seborrhoeic eczema treated?

A

ketoconazole shampoo or topical imidazole cream

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164
Q

What is scabies?

A

An intensely itchy rash caused by the sarccoptes scabies mite

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165
Q

How does scabies present?

A

Itchy red papules anywhere on the skin
Sometimes liner or curved burrows can be seen
Itch is usually worse at night

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166
Q

What complications can arise from scabies?

A

Excoriations

Secondary bacterial infections

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167
Q

How is a diagnosis of scabies confirmed?

A

Skin scrapings and examining a potassium hydroxide preparation by microscopy for the mites and/or eggs

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168
Q

How is scabies treated?

A

Topical scabicide is applied and washed off after 10 hours (all skin below the neck)
In under 2s treat head and neck aswell
All close contacts should be treated even if they are asymptommatic

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169
Q

How does crusted (Norwegian) scabies differ from regular scabies?

A

Occurs in immunospressed people where huge numbers of mites are carried. It is not always itchy but is extremely effective.

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170
Q

How does Norwegian scabies present?

A

Hyperkeratotic crusted lesions

May progress to widespread erythema with irregular crusted plaques.

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171
Q

How is Norwegian scabies treated?

A

Careful barrier nursing
Repeated applications of a scabicide
Oral invermectin

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172
Q

What are lice?

A

Blood sucking ectoparasites that can affect humans in 3 ways.

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173
Q

How do headlice present?

A

Itch
Scalp excoriations
Papules on the neck

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174
Q

How are headlice diagnosed?

A

The presence of eggs stuck to the hair shaft

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175
Q

How are headlice treated?

A

eradication difficult due to non-compliance and resistance

Malathion, carbaryl and phenothin are the most commonly used agents (insecticides)

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176
Q

How do body lice present clinically?

A

Itch
Excoriations
post-inflammatory hyperpigmentation of the skin
Infestation of poverty and neglect

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177
Q

How should body lice be treated?

A

malathion/permethrin for patient and high temp washing and drying of clothing

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178
Q

How do pubic lice present?

A

Itching esp. at night

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179
Q

How are pubic lice treated?

A

Malathion, carbaryl and phenothin are the most commonly used agents (insecticides)

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180
Q

How do arthropod-borne diseases (insect bites) preset?

A

itchy urticated lesions, often grouped in clusters

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181
Q

How can eczema present histologically?

A

A collection of fluid in the epidermis between keratinocytes (spongiosis) and an upper dermal peri-vascular infiltrate of lymphohistiocytic cells

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182
Q

How can chronic eczema present histologically?

A

marked thickening of the epidermis (acanthosis)

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183
Q

What is the prevalence of atopic eczema?

A

Common - upto 5% of UK

10-20% children

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184
Q

What is the initial pathophysiological process of atopic eczema?

A

Selective activation of Th2CD4 lymphocytes driving the inflammatory processes

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185
Q

What cells predominate the chronic phase of atopic eczema?

A

Th0 and Th1

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186
Q

What immunoglobulin is raised in 80% of patients with atopic eczema?

A

IgE

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187
Q

What is fillagrin?

A

An epidermal barrier protein

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188
Q

How is it thought that having a mutation in the filaggrin gene can predispose an individual to atopic eczema?

A

Mutations can cause ichthyosis vulgaris which can predispose Caucasians to atopic eczema.

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189
Q

What things may exacerbate atopic eczema?

A 
Infections
Lack of infant infection
Chemicals/detergents
Teething, stress, anxiety
Cat + dog fur
Foods and house mites
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190
Q

How does atoptic eczema most commonly present?

A

Itchy, erythematous, scaly patches esp. in flexures

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191
Q

Where does atopic eczema start in infants?

A

Head and face

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192
Q

What differences may acute lesions in atopic eczema show?

A

Weeping or exudate and small v present?esicles

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193
Q

What ca a chronic scratching in atopic eczema lead to?

A

Lichenification with exaggerated skin margins

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194
Q

In patients with pigmented skin, how would atopic eczema present?

A

Extensor involvement
May be papular or follicular in nature
Post-inflammatiry hyper or hypo pigmentation may occur and this is usually very slow to resolve

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195
Q

Other than the itchy lesions associated with atopic eczema, how else may it affect the skin?

A

Upper arm and thigh skin may feel roughened due to follicular hyperkeratosis
Palms have prominant skin creases
May be a dry fish-like scaling on lower legs (ichthyosis vulgaris)

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196
Q

If a patient with atopic eczema gets a secondary infection on some lesions, what is the causative organism most likely to be?

A

Staph aureus

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197
Q

How would a secondary infection of staph aureus to atopic eczema present?

A

Crusted, weeping, impetigo-like lesions

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198
Q

Why are cutaneous viral infections widespread when they infect atopic eczema lesions?

A

Due to sratching

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199
Q

If HSV infects areas of atopic eczema, what is this condition called?

A

eczema herpeticum

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200
Q

How does eczema herpeticum present?

A

Multiple, small blisters or “punched-out” crusted lesions associated with malaise and pyrexia

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201
Q

How is eczema herpeticum treated?

A

Rapid oral or IV aciclovir

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202
Q

What signs can appear in the eyes of somebody with atopic eczema?

A

Conjunctival irritation
keratoconjunctivitis
Cataract

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203
Q

If a child has chronic-severe atopic eczema what clinical sign may become apparent as they grow older?

A

Retarded growth (nothing to do with steroids!!)

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204
Q

How is atopic eczema diagnosed?

A

Clinically based on examination and history

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205
Q

How is the atopic part of atopic eczema diagniosed?

A

High serum IgE or high specific IgE to antigens

Also blood eosinophilia in 80% patients

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206
Q

If a patient has atopic eczema as a child, what are the chances it will spontaneously resolve before they reach their teenage years?

A

80-90%

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207
Q

What general lifestyle measures can be used to treat atopic eczema?

A

Avoiding irritants
Cotton clothing
Avoiding overheating
Potentially avoiding dairy and eggs in the under 1s

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208
Q

What is the commonly used triple therapy of topical agents used to treat atopic eczema?

A

Topical steroid
Frequent emolients
Bath oil and soap substitutes

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209
Q

What potency of steroids should be used on the face in atopic eczema?

A

ONLY mild steroids

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210
Q

What potencies of steroids may be used on the body in a patient with atopic eczema?

A

Mild
Moderate
Diluted potent

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211
Q

Potent and very potent steroids may need to be used on what body areas in atopic eczema?

A

Palms and soles (thicker skin)

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212
Q

What topical immunomodulators can be used in the treatment of atopic eczema in individuals >2y/o?

A

Tacrolimus ointment

Pimecrolimus cream

213
Q

When using immunomodulators for atopic eczema, what should patients avoid?

A

Sun exposure

Vaccines

214
Q

In patients with atopic eczema what sedating antihistamine may be used at night time?

A

Oral hydroxyzine hydrochloride

215
Q

Paste bandaging can be useful in atopic eczema with what features?

A

Resistant or lichenified

216
Q

What second-line agents can be used in atopic eczema esp. if the symptoms are affecting the patients day to day living?

A

UV phototherapy
Prednisolone
Ciclosporin
Azathioprine

217
Q

What does ciclosporin do within the immune system?

A

Inhibits IL2 production by T cells

218
Q

Is ciclosporin sfae for use in pregnancy?

A

NO!

219
Q

How does discoid (nummular) eczema present?

A

Well-demarcated, scaly, patches esp on limbs

220
Q

Atopic eczema follows a rather chronic pattern, what pattern does discoid eczema follow?

A

Acute/subacute often with an infective component (Staph. aureus)

221
Q

How does hand eczema present?

A

Itchy vesicles or blisters on the palms and sides of fingers.
Diffuse erythematous scaling and hyperkeratosis of palms
Scaling and peeling of skin esp. at fingertips

222
Q

What investigation should be performed in individuals with hand eczema as 10% will have a +ve result?

A

Patch testing

223
Q

What is seborrhoeic eczema?

A

An overgrowth of pityrosporum ovale and a strong cutaneous immune response to yeast
Affects body areas rich in sebaceous glands

224
Q

How does seborrhoeic eczema present in general?

A

Inflammation and scaling

225
Q

What conditions is seborrhoeic eczema more likely to occur in?

A

Parkinsonism and HIV

226
Q

What 3 groups of people are most often affected by seborrhoeic eczema?

A

Neonates
Young adults (esp. males)
Elderly

227
Q

How does seborrhoeic eczema present in neonates?

A

Yellowish thick crusts on the scalp (cradle cap)
More widespread erythematous, scaly rash over the trunk (esp. nappy area)
There is little pruritus
Improves spontaneously over a few weeks

228
Q

How does seborrhoeic eczema present in young adults?

A

More persistent rash than in neonates
Erythematous scaling along sides of nose, eyebrows, around the eyes and extending into the scalp
May cause inflammation of the eyelid (blepharitis)
May affect skin over sternum, axillae, groins and glans penis

229
Q

How does seborrhoeic eczema present in the elderly?

A

Widespread inflammation and scaling and potentially causing erythroderma

230
Q

What is erythroderma?

A

Erythema and scaling affecting nearly the entire skin surface

231
Q

How is seborrhoeic eczema treated?

A

Mild steroid ointment and a topical antifungal

Emolients and a soap substitute are useful adjuncts

232
Q

What treatments can be used for seborrhoeic eczema on the scalp?

A

Ketoconazole shampoo and arachis oil

233
Q

What is venous (stasis) eczema?

A

Eczema which occurs alongside chronic venous hypertension and slow movement of blood in the lower limbs

234
Q

Who is venous eczema most likely to affect?

A

Older patients esp. women and those with a PMH of venous thrombosis or previous varicose vein surgery.

235
Q

How does venous eczema present?

A 
Brownish pigmentation (due to haemosiderin) in the skin, potentially ulceration or varicose veins
Superimposed contact eczema usually due to allergic reactions to the topical therapies used.
236
Q

If a leg ulcer is resistant to treatment, what test should ALWAYS be done?

A

Patch testing to the agents used

237
Q

How is venous eczema treated?

A

Emollients and a moderately potent to potent topical steroid

Support stockings/compression bandages and leg elevation to improve the underlying venous hypertension

238
Q

Where and when does asteatotic eczema commonly affect?

A

Lower legs and backs of hands esp. in winter

239
Q

How does asteatotic eczema present?

A

Dry, plate-like cracking of the skin with a red, eczematous component.

240
Q

How is asteatotic eczema treated?

A

Avoidance of soaps
Regular emollient and bath oil use
If skin is v. inflammed then a mild topical steroid can be used

241
Q

What presentation of eczema would make you think it could be allergic/irritant contact eczema?

A

An unsual or localised distribution esp. if there is no FH of atopy.
Also an exaccerbation within the workplace

242
Q

By what 2 mechanisms can allergic/irritant contact eczema arise?

A

Direct irritation

Type IV delayed hypersensitivity

243
Q

What are the common agents to cause allergic contact eczema?

A 
Nickel
Chromate
Latex
Perfumes
Plants
244
Q

What is the usual culprit in irritant contact eczema?

A

Occupational irritants

245
Q

How is allergic/irritant contact eczema treated?

A

As for atopic eczema

Strict avoidance of any causative agent

246
Q

What is photosensitive eczema?

A

A relatively rare condition where eczema occurs in exposed areas in response to sunlight.

247
Q

How does photosensitive eczema present?

A

Typical eczema features and marked skin thickening.

248
Q

Histologically hoe does photosensitive eczema present?

A

Atypical cellular structure which may appear lymphoma-like

249
Q

How is photosensitive eczema diagnosed?

A

Using special monochromator light testing

250
Q

How is photosensitive eczema treated?

A

Avoidance of sunlight
Topical steroids + emollients in mild cases
Oral prednisolone in more severe cases
Azathioprine for long term immunosuppression
Low-dose phototherapy may desensitise an individual to the condition

251
Q

What is Lichen simplex?

A

A disorder characterised by chronic scratching or rubbing in the absence of an undrlying dermatosis

252
Q

How does lichen simplex present?

A

Thickened, scaly, hyperpigmented areas of lichenification
Starts as intense itching, and becomes more tender as the rubbing/scratching continues
Itch-scratch cycle

253
Q

What body sites does lichen simplex commonly affect?

A 
nape of neck
Lateral calves
upper thighs
upper back
scrotum
vulva
254
Q

What body sites does lichen simplex commonly affect?

A 
nape of neck
Lateral calves
upper thighs
upper back
scrotum
vulva
255
Q

What is nodular prurigo?

A

Similar to lichen simplex but has a different cutaneous response to scrtaching/rubbing

256
Q

How does nodular prurigo present?

A

Individual, itchy papules and domed nodules esp. on teh upper trunk and extensor surfaces of limbs

257
Q

What can predispose an individual to either lichen simplex or nodular prurigo?

A

Being Asian, Black African or Oriental
Atopic history
Emotional stress

258
Q

How are lichen simplex and nodular prurigo treated?

A

Very potent topical steroids with occlusive tar bandaging
Immunosupression for v. resistant cases
Phototherapy may also be of benefit

259
Q

What is psoriasis?

A

A common papulo-squamous disorder characterised by red, well-demarcated, scaly patches

260
Q

When does psoriaris commonly present?

A

In 16-22 y/os (commoner)

55-60 (late onset)

261
Q

What is the aetiology behind psoriasis?

A

Polygenic + environmental

Evidence suggests a T-cell driven disorder to unidentified antigens

262
Q

Briefly explain the pathogenesis behind psoriasis.

A

Trigger factors activate dendritic cells, which produce Th1 and Th17.
These secrete mediators to act on keratinocytes to release chemokines, cytokines etc.
These maintain the inflammation and feedback to the dendritic cell.
This results in upregulation of Th1-type T-cell cytokines, growth factors and adhesion molecules.

263
Q

What does psoriasis show on histology?

A

Epidermal acanthosis and parakeratosis
Granular layer often absent
Rete ridges are elongated and clubbed
Capillary dilatation surrounded by a neutrophilic and lymphohisteocytic perivascular infiltrate

264
Q

What does psoriasis show on histology?

A

Epidermal acanthosis and parakeratosis
Granular layer often absent
Rete ridges are elongated and clubbed
Capillary dilatation surrounded by a neutrophilic and lymphohisteocytic perivascular infiltrate

265
Q

What drugs can worsen the presentation of psoriasis?

A

Lithium
Beta blockers (rare)
Anti-malarials

266
Q

How does chronic plaque psoriasis present?

A

Pink/red scaly patches with a silver scale
Extensor surfaces, lower back, ears and scalp are commonly affected
Lesions can become itchy or sore

267
Q

What it Kobner’s phenomenon?

A

New lesions appear at sites of skin trauma (psoriasis and other conditions)

268
Q

How does flexor psoriasis present?

A

Tends to arise in later life
Well-demarcated, red glazed plaques confined to the flexures (no scaling)
Often misdiagnosed as a candidal infection (but candida has satellite lesions)

269
Q

How does guttate psoriasis present?

A

‘Raindrop-like’ psoriasis seen in children and young adults

Explosive eruption of very small ovular/circular plaques appear on the trunk about 2 weeks after a strep sore throat

270
Q

How do erthyrodermic and pustular psoriasis present?

A

Most severe type representing a widespread intense inflammation of skin
Can occur together (Van Zumbusch) psoriasis
May be associated with malaise, pyrexia and circulatory disturbance
Pustules are not infected but rather sterile collections of inflammatory cells

271
Q

What nail changes can occur with psoriasis?

A

Pitting of nail plate
Distal separation of nail plate (onycholosis)
Yellow-brown discolouration
Sublingual hyperkeratosis

272
Q

What percentage of psoriasis sufferers will develop psoriatic arthritis?

A

5-10%

273
Q

What percentage of psoriasis sufferers will develop psoriatic arthritis?

A

5-10%

274
Q

How is chronic plaque psoriasis treated?

A 
Emollients - hydration
Mild-moderate topical steroids
Vit D3 analogues
Retinoids
Purified coal tar
Salicyclic acid
275
Q

What risk can occur with overuse of Vit D3 analogues?

A

Hypercalcaemia

276
Q

What are the problems with dithranol being used to treat psoriasis?

A

Irritates normal skin

Difficult to apply at home

277
Q

What can either dithranol or coal tar be combined with to give 75% clearance rates at 6 weeks?

A

UVB or PUVA therapy

278
Q

How is flexural psoriasis treated?

A

Mild steroids and/or topical tar creams

Calcitrol (Vit D3 analogue) and 0.1% tacrolimus can be used where irritation is an issue

279
Q

How is guttate psoriasis treated?

A

Topical therapies and/or UVB phototherpy

280
Q

How is palmo-plantar psoriasis treated?

A

Very potent topical steroids, coal tar paste or local had/foot PUVA
Immunosupressive agents can be used in more resistant cases

281
Q

How is palmo-plantar psoriasis treated?

A

Very potent topical steroids, coal tar paste or local had/foot PUVA
Immunosupressive agents can be used in more resistant cases

282
Q

How is erythrodermic psoriasis treated?

A

Systemic therapy but not phottherapy
Methotrexate
Cytokine modulators

283
Q

How can the severe nausea associated with methotrexte use be lessened?

A

Folic acid

284
Q

What regular blood tests need to be done in methotrexate use?

A

Monitoring for bone marrow suppression

Monitoring for liver damage (hepatic fibrosis)

285
Q

What should be avoided in methotrexate use?

A

Alcohol

NSAIDs

286
Q

What is the prognosis for patients with psoriasis?

esp guttate psoriasis

A

Most will have disease for life but 80% will have periods of remission
Severity fluctuates
Guttate psoriasis resolves spontaneously and a third will not get recurrence. The other 2/3 will get recurrent attacks or go on to develop chronic plaque psoriasis

287
Q

What is urticaria?

A

A common skin condition characterised by acute development of itchy wheals or swellings in the skin due to leaky dermal vessels.

288
Q

What is angio-oedema?

A

Similar to urticaria but involves sub-dermal vessels rather than dermal vessels

289
Q

What is the pathogenesis behind urticaria?

A

Degranulation of cutaneous mast cells releases inflammatory mediators incl. histamine
This creates the dermal and sub-dermal vessel leakiness
Most cases have an underlying AI cause

290
Q

What factors can contribute to an individual developing urticaria?

A

Secondary to infection, drug reactions, food allergy or SLE (rare)
Atopic history
Children and young adults - usual age of presentation

291
Q

In heriditary angio-oedema and ACEI-induced angio-oedema; histamine is not the key mediator. What is?

A

Bradykinin

292
Q

How does urticaria commonly present?

A

Cutaneous swellings or wheals developing over minutes
Can occur for minutes-hours before resolving spontaneously
Anywhere on body
Lesions are intensely itchy
Normally lesions are erythematous

293
Q

How does urticaria commonly present?

A

Cutaneous swellings or wheals developing over minutes
Can occur for minutes-hours before resolving spontaneously
Anywhere on body
Lesions are intensely itchy
Normally lesions are erythematous

294
Q

How does angio-oedema commonly present?

A

Soft tissue swelling esp. around eyes, lips and hands
Rarely itchy
Dangerous if mouth/larynx involved - thankfully this is rare

295
Q

What is a physical urticaria?

A

Urticaria caused by a physical stimuli e.g. cold, pressure, water, chemicals etc.

296
Q

How does cholinergic (stress/heat) urticaria present?

A

Small itchy papules appear on the upper trunk

Common

297
Q

How does delayed pressure urticaria present?

A

Deep swellings some hours after pressure has been removed (e.g. tight belt)
Rare

298
Q

What investigations are done for urticaria/angio-oedema?

A

History - most useful

Routine investigations are unjustified unless history suggests a clear cause

299
Q

How are urticarias/angio-oedema treated?

A

Underlying causes if identified should be treated
Avoidance of salicylates and opiates as they cause further mast cell degranulation
Oral antigistamines useful in idiopathic cases
If resistant to antihistamine therapy - H2 bloker or dapsone may be used

300
Q

If angio-oedema is affecting the mouth/throat what treatment is required?

A

Urgent IM adrenaline and IV steroids

301
Q

What is the general prognosis for urticarias?

A

Most idiopathic cases disappear spontaneously with the majority controlled by antihistamines
Physical urticarias are more persistent and more resistant to therapy

302
Q

What is urticarial vasculitis and when should it be suspected?

A

A urticaria varient

If individual lesions last >24h and leave bruising then suspect

303
Q

What symptoms are associated with urticarial vasculitis?

A

Arthralgia or myalgia

Small % may go onto develop an AI rheumatic disease

304
Q

How is urticarial vaculitis diagnosed?

A

Skin biopsy

305
Q

What investigations should be done in urticarial vasculitis?

A

Full vasculitis screen for an underlying cause

306
Q

How is urticarial vasculitis treated?

A

Antihistamines
Oral Dapsone
Immunosuppressants

307
Q

How is urticarial vasculitis treated?

A

Antihistamines
Oral Dapsone
Immunosuppressants

308
Q

What is lichen planus?

A

A pruritic inflammatory dermatosis commonly associated with mucosal involvement.

309
Q

What is the possible pathogenesis behind lichen planus?

A

T-cell driven reaction

310
Q

How does lichen planus present histologically?

A

Hyperkeratosis with thickening of granular cell layer
Dense T-cell infiltrate at the DEJ - becomes ragged and saw-toothed
Basal layer shows liquefactive degeneration with colloid bodies in the upper dermis.

311
Q

What is acanthosis?

A

Diffuse epidermal hyperplasia

312
Q

What is hyperkeratosis?

A

is thickening of the stratum corneum (keratin layer)

313
Q

What is hyperkeratosis?

A

is thickening of the stratum corneum (keratin layer)

314
Q

How does lichen planus present?

A

Small, purple, flat-topped, polygonal papules
Intensely itchy
Common on wrist flexors and lower legs
May be a fine, white, lacy pattern on lesion surface
Lesions often localise themselves to scratch marks

315
Q

How may lichen planus present in an individual with pigmented skin?

A

lesions fuse into plaques

Hyperpigmentation

316
Q

How might lichen planus present on the scalp?

A

Scarring alopecia

317
Q

If lichen planus involves the mucousal surfaces, how dies this present?

A

Lacy, white streaks or ulceration or white plaques

Severe pain

318
Q

How can lichen planus affect the nails?

A

Dystophy

May be lost all together in severe disease

319
Q

How can lichen planus affect the nails?

A

Dystophy

May be lost all together in severe disease

320
Q

What is the prognosis of lichen planus?

A

Often clears after 18 months but can reccur
Hypertrophic, atrophic and mucosal-involving varients are more persistent and may last for years
Ulcerative mucosal disease is pre-malignant

321
Q

How is lichen planus treated?

A

Potent topical steroid

322
Q

How is lichen planus treated?

A

Potent topical steroids and sometimes oral prednisolone
Oral lesions need high potency steroids given as a gel, ointment or mouth wash
Resistant cases may respond to PUVA, oral retinoids or azathioprine
Topical 0.1% tacrolimus ointment or pimecrolimus is v. useful in oral disease that has not responded to steroids

323
Q

Although the cause of acne vulgaris is multifactorial, what critical factors play a part in the pathological process?

A

Follicular epidermal hyperproliferation
Blockage of pilosebaceous units with surrounding inflammation
Increased sebum production
Infection with Propionbacterium acnes.

324
Q

How does infection with propionbacterium bacterium cause inflammation?

A

Activates Toll-like receptor 2, leading to production of pro-inflammatory cytokines

325
Q

Where does acne vulgaris present on the body?

A

Areas rich in sebaceous glands such as the face, back and sternal area

326
Q

What are the 3 cardinal features of acne vulgaris?

A

Open comedones (blackheads) or closed comedones (whiteheads
Inflammatory papules
Pustules

327
Q

If inflammed acne lesions rupture what can this cause?

A

Deep-seated dermal inflammation

328
Q

If inflammed acne lesions rupture what can this cause?

A

Deep-seated dermal inflammation

329
Q

What is infantile acne?

A

Facial acne in infants, which may be cystic
Thought to be due to maternal androgens
Resolves spontaneously

330
Q

What is steroid acne?

A

Acne which occurs secondary to corticosteroid therapy or Cushing’s syndrome
Often appears as a pustular folliculitis on the trunk without comedomes

331
Q

What is oil acne?

A

An industrial disease seen in workers who have prolonged contact with oils or other hydrocarbons
Common on the legs and other exposed sites

332
Q

What is acne fulminans?

A

A rare variant commonly seen in young male adolescents

A severe, necrotic, crusted acne associated with malaise, pyrexia, arthralgia and bone pain

333
Q

How is acne fulminans treated?

A

Urgent oral prednisolone and analgesics followed by a course of oral isotretinoin

334
Q

What is acne conglobata?

A

A cystic acne with abscesses and interconnecting sinuses

335
Q

What is acne excoriee?

A

A deeply excoriated and picked acne with associated scarring

Much more common in females

336
Q

What is the follicular occlusion Triad

A

A rare disorder most commonly seen in black Africans
Characterised by the presence of severe nodulocystic acne, dissecting cellulitis of the scalp and hidradentis suppurativa
May be caused by a problem with follicular occlusion

337
Q

What are the 1st line agents used in acne treatment?

A

Topical keratolytics/topical retinoids/ retinoid-like agents

Topical antibiotics for inflammatory acne

338
Q

What is the 2nd line therapy for acne treatment?

A

Low dose oxytetracycline for 3-4 months minimum

Cyproterone acetate - contraceptive pill with anti-androgen activity

339
Q

What is the 2nd line therapy for acne treatment?

A

Low dose oxytetracycline for 3-4 months minimum

Cyproterone acetate - contraceptive pill with anti-androgen activity

340
Q

What 3rd line therapy is available for use in acne treatment?

A

Oral retinoids (isotretinoin)

341
Q

What are the indications for using 3rd line acne therapy?

A

If 1st and 2nd line treatments have been tried and have failed
Nodulocystic acne with scarring
Severe psychological disturbance

342
Q

What are retinoids?

A

Synthetic Vit A analogues which affect cell growth and differentiation

343
Q

What adverse effects do retinoids have?

A

V. teratogenic
Hair thinning
Myalgia
Dry skin

344
Q

How effective are retinoids?

A

> 90% will respond to therapy

65% will obtain a long term “cure”

345
Q

What needs to be carefully monitored while using retinoids?

A

Blood count
Liver biochemistry
Fasting lipids

346
Q

What is rosacea?

A

A common inflammatory rash predominently affecting the face
Onset is usually middle age and ommoner in women
Often causes significant psychological distress

347
Q

What is the suggested pathogenesis behind rosacea?

A

An underlying problem in the vasomotor stability of blood vessels
A possible role of the skin mite dermodex

348
Q

How does rosacea present clinically?

A

Facial flushing with inflammatory papules and pustules affecting the nose. forehead and cheeks
No comedomes
Dilated blood vessels, inflammation of the eyelid margins, keratitis and sebaceous gland hypertrophy (nose) can also occur

349
Q

What may exacerbate flushing in rosacea?

A 
Alcohol
Hot drinks
Sunlight
Changes in the ambient temperature
Steroids may also exacerbate or trigger the condition
350
Q

How is rosacea treated?

A

Long term use of topical metronidazole or topical azelaic acid
3 months of oral tetracycline may be useful
Cosmetic camouflage
Resistant cases may require oral metronidazole or isotretinoin

351
Q

What is perioral dermatitis?

A

A common rash which occurs around the mouth (esp. in young females)
Often has an iatrogenic component from an exacerbation from topical steroids
Exact cause is unknown

352
Q

How does perioral dermatits present?

A

Erythema, scaling, papules and occasionally pustules around the mouth
Usually spares a halo of skin immediately around the lips

353
Q

How is perioral dermatitis treated?

A

Stopping of topical steroids

3-4 month course of low-dose oxytertracycline or erythromycin and topical metronidazole

354
Q

How is perioral dermatitis treated?

A

Stopping of topical steroids

3-4 month course of low-dose oxytertracycline or erythromycin and topical metronidazole

355
Q

What happens in porphyria cutanea tarda (PCT)?

A

A bullous eruption on exposure to sunlight which heals with scarring

356
Q

What can precipitate PCT?

A

Alcohol
Hep C
HIV
Liver disease (tumours)

357
Q

How is PCT diagnosed?

A

With the presence of increased urinary uroporhyrin

358
Q

How does PCT present histologically?

A

Sub-epidermal blisters with perivascular deposition or periodic acid-Schiff-staining material

359
Q

How is PCT treated?

A

Treat the underlying diseases and relieving the skin disease

360
Q

What is erythropoietic poriotoporphyria (EPP)?

A

Irritation and burning pain in the skin on exposure to sunlight
Potential protoporphyrin deposition in the liver

361
Q

How is EPP diagnosed?

A

Fluorescence of the peripheral RBCs and by increased protoporphyrin present in RBCs and stools

362
Q

How are acute attacks of photocutaneous porphyrias treated?

A

Symptomatic treatment
Venesection to reduce urinary porphyria in PCT
Chloroquine to aid uroporphyrin excretion in PCT
Liver transplantation may be needed in severe cases

363
Q

How are attacks of photocutaneous porphyrias prevented?

A

Avoidance of sunlight
Use of zinc-containing suncreams
Oral beta-caroten provides effective protection against solar sensitivity in EPP

364
Q

What is phototherapy used for?

A

UVB and UVA both have a suppressive effect on cutaneous inflammation and may suppress systemic immunoreactivity

365
Q

What are the disadvantages of phototherapy?

A

Skin aging

May predispose to malignancy of skin (UVB less carcinogenic)

366
Q

UVA must be used alongisde what to be effective?

A

A photosensitisor agent (PUVA)

367
Q

UVA must be used alongisde what to be effective?

A

A photosensitisor agent (PUVA)

368
Q

What is a polymorphic light eruption (PLE)?

A

The most common photosentitive eruption in temperate regions affecting 10-20% of the population
Most common in young women

369
Q

How does PLE present?

A

Itchy rash after exposure to sunlight, lesions may be papules, vesicles or plaques
May last for hours-days
Starts in spring and improves in summer due to skin ‘hardening’

370
Q

How is PLE treated?

A

Avoidance of sunlight and use of sunblocks
Topical steroids help during a attack
Oral prednisolone may prevent or treat an attack caused by intense sun exposure
Resistant cases may requires desensitisation with PUVA

371
Q

What is solar urticaria?

A

An extremely rare condition where itchy urticarial lesions occur within minutes of sun exposure and settle after 1-2 hours

372
Q

How is solar urticaria treated?

A

Sun avoidance
Sunblocks
H1 antihistamines
Low dose phototherapy

373
Q

What is pemphigus vulgaris?

A

A potentially fatal blistering disease occuring in all races

Onset is usually in middle age and there is no gender preference

374
Q

What is the pathogenesis behind pemphigus vulgaris?

A

Autoantibodies against desmosomal protein desmoglein 1+3 (expressed in skin and mucosal sufaces)
Autoantibodies can bemeasured as markers of disease activity

375
Q

What does skin biopsy show in pemphigus vulgaris?

A

A superficial intraepidermal split just above the basal layer with acantholysis (separation of individual cells)

376
Q

How does pemphigus vulgaris present clinically?

A

Mucosal involvement - oral ulceration is the presenting sign in ~50% cases
This may be followed by non-itchy flaccid (loose) blisters esp on the trunk
Blistering ususally becomes widespread but they rapidly denude (burst)
Thus pemphigus often presents with erythematous, weeping erosions

377
Q

How does pemphigus vulgaris present clinically?

A

Mucosal involvement - oral ulceration is the presenting sign in ~50% cases
This may be followed by non-itchy flaccid (loose) blisters esp on the trunk
Blistering ususally becomes widespread but they rapidly denude (burst)
Thus pemphigus often presents with erythematous, weeping erosions
Flexural lesions have a vegetative appearance

378
Q

What is Nikolsky’s sign?

A

Extension of blisters by gentle sliding pressure

379
Q

How is pemphigus vulgaris treated?

A

High-dose oral prednisolone or pulsed methylprednisolone which is often needed for life
Other immunosupressive agents e.g. azathioprine or mycophenolate mofetil
The anti-B-cell drug rituximab is useful in resistant cases
IV immunoglobulin covers the lag phase of other treatments

380
Q

What is the prognosis of pemphigus vulgaris?

A

Treatment is usually effective but upto 10% of patients die from disease complications or treatment side-effects

381
Q

What is bullous pemphigoid?

A

A more common condition than pemphigus which presents later in life and mucosal involvement is rarer

382
Q

What is bullous pemphigoid?

A

A more common condition than pemphigus which presents later in life and mucosal involvement is rarer

383
Q

What does skin biopsy show in bullous pemphigoid?

A

A deeper blister due to a subepidermal split through the basement membrane

384
Q

What does skin biopsy show in bullous pemphigoid?

A

A deeper blister due to a subepidermal split through the basement membrane

385
Q

What do immunoflourescence (IMF) studies show in Bullous pemphigoid?

A

Linear staining of IgG along the basement membrane

386
Q

What do IMF studies show in pemphigus valgaris?

A

IgG intracellular staining is within the epidermis

387
Q

How does bullous pemphigoid present?

A

Large, tense bullae appear anywhere on the skin
May be centered on an erythematous or urticated background and they may be haemorrhagic
May be v. itchy

388
Q

How is bullous pemphigoid treated?

A

High dose oral prednisolone and steroid sparing agents e.g. azathioprine or mycophenolate mofetil
Often treatment can be withdrawn after 2-3 years
Side effects of medication is common esp. as most sufferers are elderly

389
Q

How is a localised or mild version of bullous pemphigoid controlled?

A

Super potent topical steroids, oral dapsone or high dose oral minocycline

390
Q

What is dermatitis herpetiformis

A

A rare blistering disease associated with coeliac disease

391
Q

What does a skin biopsy of dermatitis herpetiformis show?

A

Subepidermal blister with neutrophil microabscesses in the dermal papillae

392
Q

What do IMF studies show in dermatitis herpetiformis?

A

IgA in the dermal papillae and patchy granular IgA along the basement membrane

393
Q

What would the jejunal mucosa show in an individual with dermatitis herpitiformis?

A

A partial villous atrophy

394
Q

How does dermatitis herpetiformis present clinically?

A

Small, intensely itchy blisters on the skin esp. on the elbows, extensor forearms, scalp and buttocks
Tops of blisters are usually scratched off thus crusted erosions are seen at presentation
Remissions and exacerbations are common

395
Q

How does dermatitis herpetiformis present clinically?

A

Small, intensely itchy blisters on the skin esp. on the elbows, extensor forearms, scalp and buttocks
Tops of blisters are usually scratched off thus crusted erosions are seen at presentation
Remissions and exacerbations are common

396
Q

How is dermatitis herpetiformis treated?

A

GF diet
Oral dapsone or sulphonamides
Oral meds can be removed if strict GF diet is adhered to

397
Q

What are the side effects of dapsone?

A

Frequently causes a mild dose-related haemolytic anaemia

Liver damage, peripheral neuropathy and aplastic anaemia are rarer complications

398
Q

What must be monitored regularly when using dapsone?

A

Blood count

LFTs

399
Q

What are melanocytic naevi?

A

Moles
Benign overgrowths of melanocytes, common in white-skinned individuals
Appear in childhood and increase in number and size during adolescence and early adulthood

400
Q

How do melanocytic naevi change over time?

A

Often start as flat brown macules with melanocytic proliferation at the DEJ (junctional naevi)
Continue to proliferate and grow down into the dermis (compound naevi) and this causes elevation of the mole above the skin surface
Pigmentation is usually even and the border is smooth
They eventually mature into a dermal naevus (cellular naevus) often with a loss of pigment

401
Q

What are blue naevi?

A

Acquired asymptomatic blue-looking moles
Forms from proliferation of melanocytes deep in the mid-dermis
Consist of pigment rich, dendritic spindle cells

402
Q

What are halo naevi?

A

Naevi with a halo of depigmentation peripherally

Show inflammatiry regression and are overrun by lymphocytes

403
Q

What is a naevus splius?

A

A skin lesion presenting with a light brown or tan maccule, which is speckled with smaller, darker maccules or papules

404
Q

What is a Spitz naevus?

A

Usually occurs in those less than 20
Consists of large spindle/epithelioid cells
Closely mimics melanoma
Vast majority are entirely benign but there is a malignant varient
Lesions are pink due to prominent vasculature
Epidermal hyperplasia seen on histology

405
Q

What is a basal cell papilloma?

A

A common benign overgrowth of the epidermal basal cell layer
May be flesh coloured, brown or black, often looks greasy (choc chip cookie appearance)
Surface is irregular, warty and lesions appear very superficial as though just stuck onto the skin

406
Q

How are basal cell papillomas treated?

A

Cryotherapy or curettage

407
Q

What is a dermatofibroma?

A

A firm, elevated, pigmented nodule which feels like a button in the skin. Peripheral ring of pigmentation sometimes seen.
Often found on legs
May be a preceding history of trauma or insect bite
Lesion consists of histiocytes, blood vessels and varying degrees of fibrosis
If symptomatic, excision required

408
Q

What is a dermatofibroma?

A

A firm, elevated, pigmented nodule which feels like a button in the skin. Peripheral ring of pigmentation sometimes seen.
Often found on legs
May be a preceding history of trauma or insect bite
Lesion consists of histiocytes, blood vessels and varying degrees of fibrosis
If symptomatic, excision required

409
Q

What is seborrhoeic keratosis?

A

More or less the same as a basal cell papilloma
V.common in aging skin esp. on the face and trunk
Histologically shows epidermal acanthosis, hyperkeratosis and horn cysts
An eruptive appearance of many lesions may indicate an internal malignancy (Leser-Trelat sign)

410
Q

What are ephilides?

A

Freckles!
A patchy increase in melanin pigmentation which occurs after UV exposure
Reflects a clumpy distribution of melanocytes

411
Q

What is keratoacanthoma?

A

A rapidly growing epidermal tumour which develops central necrosis and ulceration
Occurs on sun exposed skin in later lifeand may grow to 2-3cm diameter
May resolve spontaneously over a few months
Better to be excised to exclude a squamous cell carcinoma, which they can mimic, and also this improves the cosmetic outcome

412
Q

What is a cherry angioma?

A

Benign angiokeratoma that appears as tiny pin-point papules esp. on trunk
Increase in frequency with age
No treatment is required

413
Q

What are solar keratoses (actinickeratoses)

A

Frequently develop in later life in white-skinned individuals with significant sun exposure
Appear on skin as erythematous, silver-scaly papules or patches with a conical surface and a red base
Background skin is often inelastic, wrinkled and may show flat, brown macules (solar lentigos) reflecting diffuse solar damage

414
Q

What may happen to a small proportion of solar keratoses after being present for many years?

A

Turn into SCCs

415
Q

How are solar keratoses treated?

A

Cryotherapy
Topical 5-fluorouracil crsm
5% imiquimad cream
Diclofenac gel

416
Q

What is Bowen’s disease?

A

A form of carcinoma-in-situ which may rarely become invasive

Thought to be due to long term sun exposure

417
Q

What is Bowen’s disease?

A

A form of carcinoma-in-situ which may rarely become invasive
Thought to be due to long term sun exposure
Commoner in immunospressed individuals

418
Q

How does Bowens disease present?

A

Isolated, scaly, red patch or plaque similar to psoriasis but with a v. irregular border
Lesions slowly increase in size with time
May involve epidermis of the mucosa or neighbouring skin
Nonspecific erythema or a warty thickening

419
Q

What areas of the body does Bowen’s disease commonly affect?

A

Sun exposed areas esp. womens legs

Also vulva, glans penis and perianal skin

420
Q

What disease is linked to Bowen’s disease?

A

HPV infection - higher pre-malignant potential

421
Q

How is Bowen’s disease treated?

A 
Topical 5-flurouracil
5% imiquimod cream
Cryotherapy
Curettage
Photodynamic therapy
Tissue-destructive laser
422
Q

What is atypical mole syndrome (dysplastic naevus syndrome)?

A

A large number of melanocytic naevi begin to appear in childhood even in unexposed sites
Individual lesions may be large with irregular pigmentation on border

423
Q

How does dysplstic naevus syndrome appear histologically?

A

May show cytological and architechtural atypia, but no frank malignant change

424
Q

What should individuals with dysplastic naevus syndrome be aware of?

A

They have an increased risk of developing malignant melanoma
Should have their moles photographed and regulary reviewed
Suspicious lesions should be excised?

425
Q

What should individuals with dysplastic naevus syndrome be aware of?

A

They have an increased risk of developing malignant melanoma
Should have their moles photographed and regulary reviewed
Suspicious lesions should be excised?

426
Q

What is a giant congenital melanocytic naevi?

A

A very large mole present at birth

V. large lesions >20cm show increased risk of developing malignant melanoma

427
Q

How are giant congenital melanocytic naevi managed?

A

Excision is considered but the cosmetic appearance is often not worth it
Regular monitoring
A few will improve spontaneously or partially resolve during childhood

428
Q

What is lentigo maligna?

A

A slow-growing macular area of pigmentation seen in elderly people, commonly on the face
Border and pigmentation is often irregular
Increased risk of developing a malignant melanoma

429
Q

What is the treatment for lentigo maligna?

A

Excision if possible

5% imiquimod cream tried in lesions where excision would be disfiguring

430
Q

What is a basal cell carcinoma (BCC)?

A

The most common malignant type of skin tumour.

Common in the elderly population in exposed sites

431
Q

How does a BCC present?

A

A slow-growing papule or nodule which may go on to ulcerate
Telangiectasia over the tumour or a skin-coloured jelly-like pearly edge may be seen
It grows slowly and erodes structures if left untreated but almost never metastasises

432
Q

How is a BCC treated?

A

Usually with surgical excision

Phototherapy, cryotherapy and 5%imiquimod cream can be used as adjuncts to surgery

433
Q

What is a squamous cell carcinoma (SCC)?

A

A more aggressive malignant tumour than BCC, mostly related directly to sun exposure

434
Q

What conditions may be associated with development of SCC?

A

Solar keratoses
Bowen’s disease
Lupus vulgaris - chronic inflammation

435
Q

How does SCC present clinically?

A

Lesions are often keratotic, ill-defined nodules that may ulcerate.
May grow v. rapidly

436
Q

How are SCCs treated?

A

Excision or occasionally radiotherapy

Curettage should be AVOIDED

437
Q

How are SCCs treated?

A

Excision or occasionally radiotherapy

Curettage should be AVOIDED

438
Q

What is malignant melanoma?

A

The most serious form of skin cancer, where metastases occur early and death is possible even in young people

439
Q

What predisposed an individual to developing a malignant melanoma?

A 
Excessive sunlight exposure
Pale skin
Sun sensitivity
Multiple melanocytic naevi (>50)
Immunosuppression
Dysplastic naevi syndrome
Lentigo maligna
\+ve FH
440
Q

What are the 4 clinical types of malignant melanoma?

A

Lentigo maligna melanoma
Superficially spreading malignant melanoma
Nodular Malignant melanoma
Acral lentiginous malignant melanoma

441
Q

How does lentigo maligna melanoma present?

A

A patch of lentigo maligna develops a papule or nodule, signalling an invasive tumour

442
Q

How does a superficially spreading malignant melanoma present?

A

A large, flat, irregularly pigmented lesion which grows laterally before vertical invasion occurs

443
Q

How does a nodular malignant melanoma present?

A

Most aggressive type
Rapidly growing, pigmented nodule which bleeds or ulcerates
Rarely they are amelanotic and mimic pyogenic granuloma

444
Q

How does acral lentiginous malignant melanoma present?

A

Pigmented lesions on the palm, soles or under the nail
Usually present late
May not be related to sun exposure

445
Q

What is the treatment for malignant melanoma?

A

Surgery is the only curative treatment with surgical margins

446
Q

What does the prognosis of malignant melanoma dependant on?

A

Breslow Thickness

447
Q

What is the prognosis for pTis?

A

Melanoma in situ

100% 5 year survival

448
Q

What is the prognosis for pT1?

A

Tumour less than 1mm deep

90% 5 year survival

449
Q

What is the prognosis for pT2?

A

Tumour 1-2mm deep

80% 5 year survival

450
Q

What is the prognosis for pT3?

A

Tumour 2-4mm deep

55% 5 year survival

451
Q

What is the prognosis for pT4?

A

Tumour >4mm deep

20% 5 year survival

452
Q

What is the prognosis for pT4?

A

Tumour >4mm deep

20% 5 year survival

453
Q

What is Cutaneous T-cell lymphoma?

A

A rare skin tumour which often follows a fairly benign course

454
Q

How does Cutaneous T-cell lymphoma present?

A

Scaly patches and plaques which may resemble eczema or psoriasis
Lesions often appear on the buttocks and these may come and go for many years
Occasionally disease can progress to a cutaneous nodular, or tumour stage

455
Q

What would a skin biopsy of a Cutaneous T-cell lymphoma show?

A

Invasion by atypical lymphocytes

456
Q

How is Cutaneous T-cell lymphoma treated?

A

Early disease = watch and wait, topical steroids, PUVA

Advanced disease = radiotherapy, oral retinoids, chemo, immunotherapy or electron beam therapy

457
Q

What are venous ulcers?

A

The result of sustained venous hypertension in the superficial veins
Increased pressure caused extravasation of fibrinogen through the capillary walls giving rise to perivascular fibrin deposition, leading to poor oxygenation of the surrounding skin

458
Q

Where do venous ulcers commonly present?

A

On the lower leg in a triangle above the ankles

459
Q

What clinical features may be associated with venous ulceration?

A

Oedema of lower legs
Venous eczema
Brown pigmentation from haemosiderin
Varicose veins
Lipodermatosclerosis - a fibrosing panniculitis of the subcut. tissue
Scarring white atrophy with telangiectasia (atrophie blanche)

460
Q

What is panniculitis?

A

Inflammation of subcutaneous adipose tissue

461
Q

How are venous ulcers treated?

A 
High-compression bandaging
Leg elevation
Doppler studies to exclude arterial disease
Ulcer dressings
Diuretics
Analgesia
Lifelong support stockings
462
Q

How are venous ulcers treated?

A 
High-compression bandaging
Leg elevation
Doppler studies to exclude arterial disease
Ulcer dressings
Diuretics
Analgesia
Lifelong support stockings
463
Q

What are arterial ulcers?

A

Punched-out, painful ulcers, higher on the leg or on the foot

464
Q

What can predispose an individual to an arterial ulcer?

A

Claudication in history
Hypertension
Angina
Amoking

465
Q

How does the leg present clinically with arterial ulceration?

A

Cold and pale
Absent peripheral pulses
Arterial bruits
Loss of hair may also be present

466
Q

How is arterial disease confirmed when faced with a leg ulcer?

A

Doppler studies

467
Q

How are arterial ulcers treated?

A

Keep ulcer clean and covered
Analgesia
Vascular reconstruction is needed
Compression bandaging must NOT be used

468
Q

What are pressure sores?

A

Skin ischaemia from sustained pressure over a bony prominence (heel and sacrum) in patients who are immobile.

469
Q

What is a stage 1 pressure sore?

A

Non-blanchable erythema of intact skin

470
Q

What is a stage 2 pressure sore?

A

Partial-thickness skin loss of epidermis/dermis

471
Q

What is a stage 3 pressure sore?

A

Full-thickness skin loss involving subcut. tissue but not fascia

472
Q

What is a stage 4 pressure sore?

A

Full-thickness skin loss with involvement of muscle/bone/tendon/joint capsule

473
Q

How are pressure sores prevented?

A

Specialist tissue-viability nurses identify at risk patients and train other clinical staff
Risk assessment

474
Q

How are pressure sores prevented?

A

Specialist tissue-viability nurses identify at risk patients and train other clinical staff
Risk assessment

475
Q

How are pressure sores treated?

A

Best rest with pillows and fleeces to keep pressure off bony areas
Air-filled cushions for those in wheelchairs
Pressure-relieving mattresses and beds
Regular turning
Adequate nutrition
Non-irritant, occlusive, moist dressings
Analgesia

476
Q

What is vasculitis?

A

An inflammatory disorder of the blood vessels which causes endothelial damage

477
Q

What are the cutaneous features of vasculitis?

A

Haemorrhagic papules, pustules, nodules or plaques which may erode and ulcerate
Lesions do not blanche with pressure

478
Q

What is lymphoedema?

A

A chronic non-pitting oedema due to lymphatis insufficiency which most commonly affects the legs and progresses with age

479
Q

How does lymphoedema present?

A

Chronic disease may cause a ‘cobblestine’ thickening of the skin

480
Q

How can lymphoedema occur?

A

Primary disease due to an inheriteddeficiency of lymphatic vessels
Secondary due to obstruction of lymphatuc vessels

481
Q

How is lymphoedema treated?

A

Compression stockings and physical massage

If recurrent cellulitis then long-term antibiotics are advised so lymph vessels do not become damaged

482
Q

What is lymphangioma Circumscription?

A

A rare haematoma of lymphatic tissue that presents in childhood with multiple small vesicles in the skin which weep lymphatic fluid and sometimes blood
Reflects deeper vessel involvement so surgery should be avoided

483
Q

How should lymphangioma circumscription be treated?

A

Cryotherapy

CO2 laser treatments

484
Q

What is vitiligo?

A

A common AI disease of depigmentation due to areas of melanocyte loss which presents in childhood or early adulthood

485
Q

What is vitiligo?

A

A common AI disease of depigmentation due to areas of melanocyte loss which presents in childhood or early adulthood

486
Q

How may vitiligo present?

A

Symmetrical lesions frequently involving the hace, hands and genitallia
Hair can also depigment
Trauma may induce new lesions
Spontaneous repigmentation may occur but this is rare

487
Q

How is vitiligo treated?

A

Suncreams to avoid burning
Tacrolimus ointment on face
Potent topical steroids or phototherapy may help
Monobenzone if widespread
Referral to a specialist camouflage clinic

488
Q

What is post-inflammatory hypopigmentation?

A

One of the most common causes of paled skin
May be seen as a consequence of other skin disease
If skin disease is controlled then pigmentation returns to normal over months
Post-inflammatory HYPER-pigmentation can also occur

489
Q

What is oculocutaneous albinism?

A

A group of rare autosomal recessive disorders which affects the pigmentation of skin, hair and eyes.
Melanocytes are normal in number but have abnormal function

490
Q

How does oculocutaneous albinism present?

A

Universal pale skin, white or yellow hair, pinkish iris

Photophobia, nystagmus, squint are also present in most cases

491
Q

How is oculocutaneous albinism treated?

A

Obsessive protection against sunlight

492
Q

What is idiopathic guttate hypomelanosis?

A

Occurs most often in black African people with small asymptomatic porcelain-white macules on skin exposed to sunlight
No effective treatment

493
Q

How can leprosy affect skin pigmentation?

A

Both tuberculoid and intermediate leprosies present with anaesthetic patches of depigmentation
Also loss of hair and decreased sweating

494
Q

What conditions are common causes of hyperpigmentation?

A 
Freckles
Lentigos
Cholasma
Metabolic/endocrine effects
Peutz-Jeghers disease
Urticaria pigmentosa
Cafe-au-lait macules
Multiple lentigines
Acquired melanocytic naevi
495
Q

What are lentigos?

A 
A more permanant macule of pigmentation similar to freckles but often present in the winter
Solar lentigos (liver spots) occur in older people on exposed skin due to actinic damage
496
Q

What are lentigos?

A 
A more permanant macule of pigmentation similar to freckles but often present in the winter
Solar lentigos (liver spots) occur in older people on exposed skin due to actinic damage
497
Q

What is cholasma?

A

Brown macules seen symmetrically over the cheeks and forehead
May be spontaneous but may also occur in pregnancy and in individuals taking the oral contraceptive

498
Q

What metabolic/endocrine effects can cause hyperpigmentation of skin?

A

Chronic liver disease esp. haemochromatosis
Cushing’s syndrome
Addison’s disease
Nelson’s syndrome

499
Q

What is Peutz-Jeghers syndrome?

A

An autosomal dominant condition which presents with brown macules on the lips and perioral region
Associated with GI polyposis

500
Q

What is urticaria pigmentosa?

A

Multiple pigmented macule sin children which become red,itchy and urticated if rubbed
Resolves spontaneously in children but does not if condition begins in adulthood

501
Q

What would a skin biopsy of urticaria pigmentosa show?

A

Excess of mast cells in the skin

502
Q

How is urticaria pigmentosa treated?

A

Antihistamines

Sodium cromoglicate or PUVA

503
Q

What are cafe-au-lait molecules seen in?

A 
NF 1+2
Tuberculosclerosis
Ataxia
Telangiectasia
MEN1
504
Q

In what conditions are multiple lentigines seen?

A

Peutz-Jeghers syndrome
Xeroderma pigmentosum
LEOPARD syndrome

505
Q

What is LEOPARD syndrome?

A 
L - Lentigines
E - ECG conduction abnormalities
O - Ocular hypertelorism
P - Pulmonary stenosis
A - Abnormalities of genitallia
R - Retardation of growth
D - Deafness
506
Q

In what conditions are acquired melanocyic naevi seen?

A

Tuner’s syndrome

Atypical mole syndrome

507
Q

What is toxic epidermal necrosis (TEN)?

A

A widespread subepidermal blistering and sloughing of >30% of the skin

508
Q

How does TEN present?

A

Cough, myalgia and poor appetite may precedes skin signs by 2-3 days
Skin may itch but typically burns
Fever and mucosal involvement common
Multiorgan involvement and sepsis often occurs

509
Q

How is TEN treated?

A

A specialist burns unit or ICU

Occlusive cutaneous dressings give significantly reduced pain

510
Q

What is drug-induced hypersensitivity syndrome (DHS)?

A

A serious adverse systemic reaction to a drug occuring 2-6 weeks after the initial exposure

511
Q

How does DHS present?

A 
Generalised mucocutaneous rash
Fever
Lymphadenopathy
Arthralgia
Pharyngitis
Periorbital oedema
Hepatoslenomegaly
512
Q

What may blood show when examined in DHS?

A

Peripheral eosinophillia

Lymphocytosis with atypical lymphocytes

513
Q

What is a common culprit of DHS?

A

Aromatic anticonvulsants

514
Q

How is DHS treated?

A

Drug withdrawal
Systemic steroids
Supportive care

515
Q

How is DHS treated?

A

Drug withdrawal
Systemic steroids
Supportive care

516
Q

What diseases can cause nail pitting?

A

Psoriasis
Alopecia areta
Atopic eczema
Trauma

517
Q

What conditions can cause onchylosis?

A

Psoriasis
Thyrotoxicosis
Trauma

518
Q

What diseases can cause Koilonychia?

A

Iron deficeincy anaemia

Congenital - rare

519
Q

What conditions can cause Leuconycia?

A

Hypoalbuminaemia

520
Q

What diseases can cause Beau’s lines?

A

Severe illness or shock

521
Q

What causes Yellow nail syndrome?

A

Rare disorder of lymphatic drainage

Pleural effusions, bronchiectasis and nail lymphoedema

522
Q

What can cause onychogryphosis?

A

Trauma
Psoriasis
Fungal infection

523
Q

What is androgenic alopecia?

A

The most common type of non-scarring hair loss

Male pattern baldness

524
Q

What is alopeica areata?

A

An AI-mediated type of hair loss associated with other organ specific AI diseases
Children or young adults

525
Q

What is a cream?

A

A semisolid mixture of oil and water, held together by an emulsifying agent
Have high cosmetic acceptability

526
Q

What is an ointment?

A

A semisolid containing no water and based purely on oils or greases.
Feel greasy or sticky to touch

527
Q

What are lotions?

A

Water-based or alcohol-based substance which provides a cooling effect on the skin

528
Q

What are gels?

A

Semisolid preparations of high molecular weight polymers

529
Q

What are pastes?

A

Contain a high % powder in an ointment base

x 2nd Year Medicine (10 decks)

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